Bernard Beck

The hippocampus is a brain region of primary importance for neurogenesis, which occurs during early developmental states as well as during adulthood. Increases in neuronal proliferation and in neuronal death with age have been associated with drastic changes in memory and learning. Numerous neurotransmitters are involved in these processes, and some neuropeptides that mediate neurogenesis also modulate feeding behavior. Concomitantly, feeding peptides, which act primarily in the hypothalamus, are also present in the hippocampus. This review aims to ascertain the role of several important feeding peptides in cognitive functions, either through their local synthesis in the hippocampus or through their actions via specific receptors in the hippocampus. A link between neurogenesis and the orexigenic or anorexigenic properties of feeding peptides is discussed.

We examined the gastric mucosa structure and inflammatory status in control well‐nourished Wistar dams and in Wistar dams deprived of choline, folate, and vitamin B ₁₂ during gestation and suckling periods, and in their offspring just before birth and at weaning. In this model of methyl donor deficiency (MDD), structural protein (E‐cadherin and actin) N ‐homocysteinylation was measured through immunoprecipitation and proximity ligation assays. Cellular stress, inflammation, and apoptosis were estimated by the analysis of the NF‐κB pathway, and the expression of superoxide dismutase, cyclooxygenase‐2, tumor necrosis factor α, caspases 3 and 9, and TUNEL assay. Aberrant gastric mucosa formation and signs of surface layer erosion were detected in MDD fetuses and weanlings. E‐cadherin and actin were N ‐homocysteinylated (+215 and +249% vs. controls, respectively; P P P P P P N ‐homocysteinylation, marked inflammation, and apoptosis, despite activation of repair machinery.—Bossenmeyer‐Pourié, C., Pourié, G., Koziel, V., Helle, D., Jeannesson, E., Guéant, J.‐L., and Beck, B. Early methyl donor deficiency produces severe gastritis in mothers and offspring through N ‐homocysteinylation of cytoskeleton proteins, cellular stress, and inflammation. FASEB J. 27, 2185–2197 (2013). www.fasebj.org

Prenatal nutritional conditions can predispose to development of obesity and metabolic syndrome in adulthood. Gestation with its important modifications in hormonal status is a period of changes in normal feeding habits with pulses of consumption or avoidance of certain categories of food. We tried to mimic in an animal model some changes in food consumption patterns observed in pregnant women. For this purpose, Long–Evans female rats were fed during the dark period, their usual pre-gestational food quantity, and were allowed to complete their daily intake with either a restricted control (Cr), high-fat (HF), or high-carbohydrate (HC) diet available ad libitum during the light period. Dams fed a control diet ad libitum (Ca) served as controls. Body weight and composition, food intake, and metabolic hormones (insulin, leptin) were recorded in male offspring until 20 weeks after birth. Cr and HC females ate less than Ca females (−16%; p < 0.001) and their offspring presented a weight deficit from birth until 6 (HC group) and 10 (Cr group) weeks of age (p < 0.05 or less). Plasma leptin corresponded to low body weight in Cr offspring, but was increased in HC offspring that in addition, had increased plasma insulin, blood glucose, and subcutaneous adipose tissue mass. HF dams ate more than Ca dams (+13%; p < 0.001), but plasma leptin and insulin were similar in their offspring. Hypothalamic Ob-Rb expression was increased in Cr, HC, and HF offspring (+33–100% vs Ca; p < 0.05 or less). HC supplement ingestion during gestation therefore leads to insulin and leptin resistance in adult offspring independently of lower birth weight. These hormonal changes characterize obesity-prone animals. We therefore suggest that attention should be paid to the carbohydrate snacking and overall carbohydrate content in the diet during the last weeks (or months) preceding delivery to limit development of later metabolic disorders in offspring.